CAJ | 학술논문

目的研究缺氧预处理(HPC)对创伤性脑损伤(TBI)大鼠挫伤区周围皮层脑组织缺氧诱导因子-1 α(HIF-1α)及葡萄糖转运蛋白-1(GLUT-1)表达的影响.方法 102只SD大鼠按随机数表法分为对照组(C组∶n=6)、创伤性脑损伤组(TBI组∶n=48)、缺氧预处理后创伤性脑损伤组(HPCT组∶n=48).HPCT组大鼠先置于低压氧舱行缺氧预处理(50.47 kPa,3 h/d,3 d),而后HPCT组和TBI组采用自由落体打击法建立大鼠创伤性脑损伤模型.伤后分别于1、4、8、12h和1、3、7、14d处死大鼠留取皮层脑组织标本,并分别采用RT-PCR和Westem blotting检测挫伤周围皮层HIF-1α及GLUT-1的表达情况.结果与对照组比较,TBI组伤后4h、8h、12h、1d及3 d HIF-1α和GLUT-1的表达均明显增加,差异有统计学意义(P<0.05);伤后1h、7d及14 d HIF-1α和GLUT-1的表达较对照组差异无统计学意义(P>.05).HPCT组与对照组和TBI组比较,HIF-1α和GLUT-1的表达在伤后1h即开始增加,伤后4h、8h、12h、1d、3d及7d均明显增加,差异有统计学意义(P＜0.05);伤后14 d HIF-1α和GLUT-1的表达对照组和TBI组差异无统计学意义(PP＜.05).结论缺氧预处理可提高创伤性脑损伤后脑组织的缺氧耐受性,并通过调整脑内葡萄糖代谢通路发挥脑保护作用,其机制可能与诱导皮层脑组织HIF-1α的表达,进而上调GLUT-1 mRNA及蛋白的表达有关.
목적 연구결양예처리(HPC)대창상성뇌손상(TBI)대서좌상구주위피층뇌조직결양유도인자-1 α(HIF-1α)급포도당전운단백-1(GLUT-1)표체적영향.방법 102지SD대서안수궤수표법분위대조조(C조∶n=6)、창상성뇌손상조(TBI조∶n=48)、결양예처리후창상성뇌손상조(HPCT조∶n=48).HPCT조대서선치우저압양창행결양예처리(50.47 kPa,3 h/d,3 d),이후HPCT조화TBI조채용자유락체타격법건립대서창상성뇌손상모형.상후분별우1、4、8、12h화1、3、7、14d처사대서류취피층뇌조직표본,병분별채용RT-PCR화Westem blotting검측좌상주위피층HIF-1α급GLUT-1적표체정황.결과 여대조조비교,TBI조상후4h、8h、12h、1d급3 d HIF-1α화GLUT-1적표체균명현증가,차이유통계학의의(P<0.05);상후1h、7d급14 d HIF-1α화GLUT-1적표체교대조조차이무통계학의의(P>.05).HPCT조여대조조화TBI조비교,HIF-1α화GLUT-1적표체재상후1h즉개시증가,상후4h、8h、12h、1d、3d급7d균명현증가,차이유통계학의의(P＜0.05);상후14 d HIF-1α화GLUT-1적표체대조조화TBI조차이무통계학의의(PP＜.05).결론 결양예처리가제고창상성뇌손상후뇌조직적결양내수성,병통과조정뇌내포도당대사통로발휘뇌보호작용,기궤제가능여유도피층뇌조직HIF-1α적표체,진이상조GLUT-1 mRNA급단백적표체유관.
Objective To investigate the effect of hypoxic preconditioning (HPC) on the expressions of hypoxia-inducible factor-1α (HIF-1α) and Glucose transporter-1 (GLUT-1) in cerebral cortex of rats with traumatic brain injury (TBI).Methods One hundred and two SD rats were randomly assigned to control group (n=6),TBI group (n=48) and TBI after HPC group (HPCT,n=48).The rats of HPCT group were exposed to 50.47 kPa absolutely for 3 h daily for consecutive 3 days; 24 h after the last precondition,the TBI models in the rats of HPCT group and TBI group were established with restricted free fall injury method.At each time point (1,4,8 and 12 h,and 1,3,7 and 14 d after TBI),6 rats from TBI group and HPCT group were sacrificed respectively.The brain tissues were prepared for RT-PCR and Western blotting to obsevre the semi-quantitate gene transcription and protein expressions of HIF-1α and GLUT-1.Results As compared with control group,TBI group showed increased expressions of HIF-1α and GLUT-1 4,8 and 12 h,and 1 and 3 d after TBI (P＜0.05); however,no significant difference was found at 1 h,7 and 14 d after TBI (P＞0.05).As compared with those in the TBI group and control group,the levels of HIF-1α and GLUT-1 in HPCT group began to increase at 1 h afterTBI,and markedly increased at other time points (4,8and12h,and1,3and7d) (P＜0.05); however,the expressions showed no significant difference at 14 d after TBI (P＞0.05).Conclusions HPC can improve hypoxia tolerance of brain tissues after TBI.Neuroprotection of HPC may somewhat be related to adjust the cerebral glucose metabolic pathway inducing GLUT-1 mRNA and protein expressions through up-regulating HIF-1α expression in cerebral cortex in rats with TBI.